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Pathophys > COPD/Emphysema/Chronic Bronchitis/Asthma/Cystic Fibrosis > Flashcards

COPD/Emphysema/Chronic Bronchitis/Asthma/Cystic Fibrosis Flashcards

1
Q

COPD (chronic obstructive pulmonary disease) includes what 3 things:

A
  1. Emphysema
  2. Chronic Asthma
  3. Chronic bronchitis + small airway diseases
    - > may occur independently or in combination
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2
Q

T/F Often patient with emphysema often has lung cancer

A

True

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3
Q

Risk factors of COPD? (5)

A
  1. Exposure to air pollution i.e. environmental irritants
  2. Secondhand smoke
  3. Occupational dusts and chemicals
  4. Heredity
  5. A history of childhood respiratory infections and socioeconomic status
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4
Q

COPD disease affect air flow in what way?

A

Obstruct

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5
Q

T/F COPD is a specific diagnosis.

A

False, COPD is not a specific diagnosis

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6
Q

Presenting signs of COPD:

A
  1. dyspnea
  2. sputum production
  3. Chronic cough
  4. reduced function
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7
Q

What is spirometry of lung volumes?

A
  • The most basic and frequently performed test of pulmonary of pulmonary function
  • Max amount of air expelled/1 sec
  • Diagnostic & prognostic
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8
Q

A FEV1/FVC ratio of what after a bronchodilator has been given is a diagnosis emphysema?

A

<0.7

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9
Q

What is emphysema?

A
  • Pathologic accumulation of air in the lungs
  • Disease of exhalation
  • Characterized by air trapping in the lungs
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10
Q

How does emphysema affect RV, TLC, and FVC1/FVC ratio?

A

RV - increase
TLC - increase
FVC1/FVC ratio - decrease

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11
Q

What is Alpha-1 antitrypsin (A-1AT)?

A
  • protein in blood

- synthesize by liver

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12
Q

What does Alpha-1 antitrypsin (A-1AT) do?

A
  • protects the lungs from the degrading actions of powerful enzyme called neutrophil elastase (↑ elastin degradation) and other proteases
  • A-1AT coats cells and provides protection against the neutrophil elastase
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13
Q

During periods of acute inflammation what occurs to the [ ] of Alpha-1 antitrypsin (A-1AT)?

A

Serum concentrations of A-1AT can rise many fold during periods of acute inflammation providing protection from inflammatory damage

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14
Q

How does smoking affect Alpha-1 antitrypsin (A-1AT)?

A

Smoking causes a hyperinflammatory state which means that neutrophils -> lots of elastase and reduced effectiveness of A-1AT

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15
Q

How does an Alpha-1 antitrypsin (A-1AT) deficiency cause general damage?

A
  • Lungs lack alpha-1 antitrypsin coating leaving them open to damage by neutrophil elastase
  • alpha-1 antitrypsin trapped in liver causing liver damage
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16
Q

A-1AT deficiency and cigarette smoking damage on the individual alveoli:

A
  • Destruction of individual alveoli
  • Development of “super” alveoli
  • Destruction of connective tissue supports for the very smallest airways allowing them to collapse during expiration
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17
Q

T/F 1 of 7 cases of emphysema are not linked to tobacco use.

A

True, A-1AT deficiency instead

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18
Q

In patient with emphysema, forced expiration causes smaller airways to collapse during expiration causing what?

A
  • air trapping in alveoli

- results in decreased alveolar Po2

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19
Q

A FEV1/FEV < what is bad news?

A
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20
Q

When alveolar attachments are destroyed by cigarette smoke, what occurs when patient exhales?

A
  • Alveolar contraction becomes increasing difficult

- Patient exhales even harder-causes collapse of small airways

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21
Q

First complaint of emphysema?

A

SOB at rest

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22
Q

Other clinical manifestations of emphysema?

A
  • Apprehensive, anxious, addicted to O2
  • Thin, cachectic
  • Deformed chest with prolonged expiration
  • Absent or non-productive cough
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23
Q

Clinical manifestations of chronic emphysema:

A
  1. Accompanying cardiac problems (cor pulmonale)
  2. Mild disease → mild hypoxemia
  3. With progression → hypoxemia worsens & CO2 is retained (hypercapnia)
  4. Chronic pulmonary metabolic acidosis
  5. Deconditioning
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24
Q

T/F Emphysema patients have a poor prognosis but PT is of benefit to them.

A

True

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25
Q

Treatment of emphysema: (7)

A
  1. reducing airway edema secondary to inflammation and bronchospasm
  2. facilitating the elimination of bronchial secretions
  3. preventing and treating respiratory infection
  4. increasing exercise tolerance
  5. avoiding airway irritants and allergens
  6. relieving anxiety and treating depression
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26
Q

Medications used for emphysema:

A 
β2 agonists or anticholinergics
anti-inflammatory agents
Antibiotics
Mucolytic expectorants
Mast cell membrane stabilizers
Antihistamines 
Glucocorticoids
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27
Q

Long term oxygen therapy for patients with emphysema:

A

Patients with PaO2 of 55 or less, or a resting oxygen saturation of 88% or less, measured at two time periods 3 weeks apart are eligible for long term O2 treatment

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28
Q

What is an oxygen concentrator?

A
  • N2 scrubber

- Increases the PO2 in the air that is inhaled

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29
Q

What should you monitor frequently when working with emphysema patient?

A

O2 pulse oximeter, HR, RR, and BP

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30
Q

The first heart sound (closing of the tricuspid and mitral valves) is best heard where on a patient with emphysema?

A
  • under the sternal area

- Hyper inflated lungs causes the heart to elongate, displacing the left ventricle downward and medially

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31
Q

What exercise program given to patient with emphysema?

A

Aerobic

HIIT

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32
Q

What is a metered-dose inhaler (MDI) used for patient with emphysema?

A

Used to deliver drugs to the lungs - must take in a slow deep breath over the course of 10 seconds while maintaining a good seal on the device and pressing on the device

33
Q

T/F Should evaluate the ability of the child or adult to correctly use the MDI

A

True

34
Q

Describe pulmonary emphysema “pink puffer”:

A
  1. Increase CO2 retention (pink)
  2. Dyspnea
  3. Ineffective cough
  4. Orthopneic
  5. Barrel chest
  6. Prolonged expiratory time
  7. speaks in short jerky sentences
  8. anxious
  9. Use of accessory muscles to breath
  10. Thin appearance
  11. Leads to right sided heart failure
35
Q

Diagnosis of chronic bronchitis:

A
  1. Productive cough lasting at least 3 months per year for 2 consecutive years
  2. FEV1/FEV < 75% (suggests obstruction) plus chronic cough suggests bronchitis
36
Q

Chronic Bronchitis characterized by:

A

Inflammation
Excessive mucus production
Scarring of lining of the bronchial tubes

37
Q

Obstruction of bronchial air flow in chronic bronchitis is caused by what?

A

increased mucus production/reduced mucus clearance

38
Q

Chronic exposure to irritants causes what in the larger bronchi?

A
  • cause mucus hypersecretion and hypertrophy of mucus-producing glands in the larger bronchi
  • Destruction of ciliary cells lining airways occurs
  • Smooth muscle hypertrophies, atrophy of epithelial cells
39
Q

If airway collapse occurs in patient with chronic bronchitis, what will occur?

A

reduced alveolar ventilation, hypoxia and acidosis

40
Q

Symptoms of chronic bronchitis:

A
  1. recurring morning cough that brings up mucus (phlegm) from the lungs
  2. Production of phlegm and chronic coughing increases both over the course of the day and as disease worsens
  3. Wheezing (high-pitched whistling noise with breathing) and is associated with narrowed airways
41
Q

T/F Chronic bronchitis symptoms are typically progressive

A

True

42
Q

Exacerbations of chronic bronchitis:

A
  1. Triggered by upper- or lower-airway infections

2. Triggered by exposure to environmental irritants, such as dust, fumes, or air pollution

43
Q

Chronic bronchitis patients tend to:

A
  1. Be polycythemic (increase RBC in blood), cyanotic, and have peripheral edema from right ventricular failure
  2. Have cor pulmonale 2O to ↑ pulmonary vascular resistance
  3. Tend to be obese
44
Q

Physical therapy implications for chronic bronchitis:

A
  1. Reduce exposure to irritants
  2. On bronchodilators (B2 agonist) and mucolytics
  3. No evidence for use of antibiotics, oral corticosteroids, expectorants, or postural drainage
  4. NSAIDs
45
Q

Describe “blue bloater” of chronic bronchitis:

A
  1. Cyanotic (blue)
  2. Cough and sputum production
  3. Hypoxia
  4. Hypercapnia (increase CO2)
  5. Acidosis
  6. Increase RR
  7. Exertional dyspnea
  8. Cor pulmonale
  9. Increase incidence in heavy cigarette smokers
  10. cardiac enlargement
  11. Use of accessory muscles to breathe
  12. High hemoglobin
  13. Digital clubbing
  14. Bilateral LE edema
46
Q

What is Episodic, reversible, obstructive lung disease characterized by bronchospasms resulting from an exaggerated inflammatory response of the airway smooth muscles to various stimuli (allergen)?

A

Asthma

47
Q

Asthma in clinically manifested by what?

A
  1. episodic dyspnea
  2. coughing
  3. wheezing
48
Q

Extrinsic asthma -

A
  • allergic reaction to specific triggers such as pollen, dust, molds, smoke, automobile exhaust, and animal dander
  • Mast cells sensitized by antibodies degranulate and release broncho active mediators after exposure to a specific antigen
49
Q

Intrinsic asthma -

A
  • Has no known allergic cause or trigger
  • Has an adult onset
  • Is most often secondary to chronic or recurrent infections of the bronchi, sinuses, or tonsils and adenoids
50
Q

Asthma inflammatory response to cellular infiltration produces what effects -

A
  1. bronchial smooth muscle spasm
  2. vascular congestion
  3. increased vascular permeability
  4. edema formation
  5. production of thick, tenacious mucus
  6. impaired mucociliary function
51
Q

Clinical course of asthma:

A
  1. Attack characterized by dyspnea with wheezing
  2. Upper airway obstruction occurs
  3. Difficulty with expiration
  4. Air trapping occurs in distal alveoli and hyperinflation
  5. Hypercapnia, acidotic
52
Q

Repeated asthma attacks cause what?

A
  1. Airway remodeling
  2. Chronic air trapping
  3. proliferation of submucosal glands
  4. hypertrophied smooth muscle
53
Q

Treatment of asthma:

A
  1. Identifying and avoiding triggers
  2. Use of bronchodilators (B2 agonists) and anti-inflammatory agents
  3. Low dose corticosteroids
54
Q

Exercise induced Bronchospasm:
What is it?
How does it subside?

A
  • airway hyperreactivity common to all persons with asthma
  • Acute, reversible, usually self-terminating airway obstruction that develops 5 to 15 minutes after vigorous intensity exercise
  • Usually the episode subsides spontaneously in 30 to 60 minutes
55
Q

Symptoms of exercise induced Bronchospasm?

A
  • coughing, chest tightness, wheezing and dyspnea, tachypnea.
  • Symptoms linked to exercise intensity
56
Q

Helpful for asthma patient to take what 20-30 minutes before exercise?

A

bronchodilators by metered-dose inhaler 20 to 30 minutes before exercise

57
Q

Corticosteroids can be used to help asthma. What are the long term effects?

A

Long term use leads to osteoporosis and muscle weakness

58
Q

What is a congenital disorder?

A

Refers to a disease or physical abnormality present from birth

59
Q

T/F Cystic fibrosis is a congenital disorder inherited in an autosomal recessive manner (both parents must be carriers)

A

True

60
Q

What is cystic fibrosis?

A
  • Genetic disease causes a disorder of ion transport (sodium and chloride) in the lungs and in the exocrine glands of the liver, pancreas, digestive, male reproductive organs (vas deferens disrupted in nearly all cases)
  • Characterized by the secretion of a thick mucous
61
Q

Cystic fibrosis predisposed an individual to what type of infections?

A
  • chronic bacterial airway infections
  • develop obstructive lung disease associated with chronic infection that leads to progressive loss of pulmonary function
62
Q

What is the most common inherited genetic disease in the white population?

A

Cystic Fibrosis

63
Q

Cystic fibrosis abnormal mucous secretion and obstruction effect on bronchi:

A

Bronchial obstruction

  1. Chronic bronchial pneumonia
  2. Generalized obstructive emphysema
64
Q

Cystic fibrosis abnormal mucous secretion and obstruction effect on Small intestine:

A

Intestinal obstruction of new born

65
Q

Cystic fibrosis abnormal mucous secretion and obstruction effect on pancreatic ducts:

A

Secondary degeneration of pancreas -> malabsorption syndrome

66
Q

Cystic fibrosis abnormal mucous secretion and obstruction effect on bile ducts:

A

biliary cirrhosis -> portal HTN

67
Q

Cystic fibrosis abnormal mucous secretion and obstruction effect on reproductive system:

A

Female - decreased fertility

Male - > 95% sterility

68
Q

What is a Cystic fibrosis transmembrane conductance regulator (CFTR) protein?

A
  • Helps to maintain the balance of salt and water on many surfaces in the body, such as the surface of the lung
  • Cl- moves to surfaces and attracts water to dilute mucus
69
Q

In patient with cystic fibrosis, CFTR protein made incorrectly or not at all. What happens then?

A

When the channel is not working correctly Cl- becomes is not transported to epithelial surfaces and remains trapped in cells -> resulting in thick mucous, salty sweat, reduced secretion of pancreatic digestive enzymes

70
Q

In patient with cystic fibrosis, thickened mucous will cause what?

A
  • decrease movement of cilia in bronchial tubes
  • Obstructs the tubular network in the pancreas which reduces release of digestive enzymes (pancreatic insufficiency) and insulin
71
Q

Cystic fibrosis progresses from mucous plugging and inflammation of small airways (bronchiolitis) to what?

A
  1. bronchitis (inflammation of the bronchial tubes)
  2. followed by bronchiectasis
  3. pneumonia
  4. fibrosis
  5. the formation of large cystic dilations
72
Q

Median survival of cystic fibrosis:

A

36.8 years

73
Q

What is most common cause of death to patient with cystic fibrosis?

A

Pulmonary failure

74
Q

How to diagnose CF?

A
  1. Genetic screening
  2. Sweat test
  3. Pancreatic elastase- a marker of pancreatic insufficiency
  4. FEV1/VC - pulmonary function tests assessing flow of air into and out of lungs
75
Q

Due to pancreatic insufficiency due to blockage of pancreatic ducts resulting in fibrosis, what can develop in the patient?

A

CF related diabetes

76
Q

How does CF affect MSK?

A
  1. Osteoporosis
  2. Muscle dysfunction
  3. Thoracic cage deformation – reduced capacity for posture and thoracic cage movement and altered spinal movement.
  4. Poorer postural control
  5. Reduced ventilation capacity
77
Q

Pharmacotherapy of CF:

A 
Bronchodilator
Hypertonic saline solutions
Pancreatic enzymes
High dose NSAIDs
Propholactic antibiotics
78
Q

PT/surgical treatment of patient with CF:

A

Therapeutic exercise
Airway clearance techniques
Lung transplants

79
Q

S&S of CF:

A
  1. Fatigue
  2. Chronic cough
  3. Recurrent URI’s (upper resp infections)
  4. Thick, sticky mucus
  5. Chronic hypoxia - clubbing, barrel chest
  6. Abdominal distention
  7. Fatty, stinky stools

Pathophys (16 decks)

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